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Protein

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Event

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A number of studies have shown that activin A expression is increased in principal neurons in the hippocampus of adult rodents in models of transient cerebral ischemia and hypoxia and also after KA treatment [1114].

However, increasedactivin A expression from surviving neurons is a potent anti-inflammatory agent that inhibits proliferation and activation of microglia and either directly and/or indirectly inhibits the gliotic response by astrocytes.

Thus, progression of neurogenesis after neurodegeneration requires the presence of an anti-inflammatory agent, either endogeneously expressedactivin A or, in its absence, an exogenously administered anti-inflammatory agent.

A subunit that makesupactivin A increased almost 24-fold in KA-treated hippocampi compared to that in hippocampi that received a control injection, although there were essentially no changes in the expression of mRNAs encoding the ?